These species play a central role in neuroinflammation by inducing oxidative stress and sustained cellular damage to DNA, proteins, and lipids. They activate microglia and trigger the release of pro-inflammatory cytokines (e.g., IL-1β, IL-6), disrupt the BBB, and modify intracellular signaling pathways such as NF-κB, perpetuating the inflammatory cascade. This contributes to cognitive deficits and fatigue [98,100,101,102,103,104,105]. This evidence concerns the gene IL1B and Cognitive impairment.